A continuation of previous studies by the applicant employing a model whereby clinically manifestable graft-versus-host disease (GVHD) can be specifically abrogated in neonatal rats by an alloantiserum (AAS) is proposed. It is also proposed to continue and extend studies both at the light microscopic and ultrastructural level on mechanisms underlying non-specific circulation deficits in neonatal rats suffering from GVHD. Because recent results demonstrating a nonspecific inhibition of lymphoid cell migration to the lymph nodes (deficient in high endothelial post-capillary venules) and spleen, with their progressive accumulation in areas of paravascular lymphoid infiltration in the liver of neonatal rats suffering from GVHD, may have profound influence on attempts to treat the syndrome, the effect of AAS treatment on such migration and morphologic defects will be investigated; as well as the temporal appearance of such of the IgG concentration with post-capillary venules of such GVHD animals. Studies will also be conducted on the effect of GVHD on a B as well as possible T lymphocyte surface membrane receptor for a site on the Fc portion of an antigen-complexed immunoglobulin molecule (the Fc receptor) as well as complement receptors. Efforts will also be made to determine the significance of recently observed higher levels of such Fc receptor lymphocytes in GVHD by examining the degree of antibody dependent and independent cytotoxicity occurring in such GVHD animals as compared to the levels of such cells and the intensity of such reactions in animals recovering from GVHD via AAS.